Why do this unless you know about the issues they cause.
Next why choose the dosing schedule that was done...two doses a year apart and if you fail you have to wait to the end of the year to be redosed.
Was it the neutralizing antibodies that drove this schedule?
Why because by the time the third dose comes along 30% of people will have pre-existing antibodies ready to stop the next dose of alemtuzumab working compared to less than 1% before the second cycle.
Of those 30% the titre (amount of antibody) of the antibody will be too low to do this, for most I suspect, but treatment failures were not mentioned in the literature. Anaphylactoid responses have not been mentioned. Do they occur as about 75% of people have binding antibodies 12 months after the second cycle. How common is this issue. I have asked numerous times.
Do you have to wait to the end of the year before the the next dose, because if you did it as disease reactivates there would be still neutralizing antibodies in the system waiting to stop the drug working as it takes a long time for them to wane..
Any way, I digress, the paper above caught my eye the take home message does not say memory B cells are the main problem. It say plasma blasts are the problem. I said I would look at papers that challenge the role of memory B cells.
Plasmablasts are the fore-runner to a plasma cell and making antibody and in this study they saw that plasmablast numbers correlate with antibody secretion.
But does this kill the memory B cell idea?
Not really as the first thing you ask is whether the memory cells are the fore-runner that change into the plasma blasts.
The answer is you cannot say that this is not the sequence.
Next why study the plasmablasts?
Because if you look at the figure above you can see that the memory B cell is the main B cell subset in the spinal fluid (there are more red dots in group 2 than group 3. But because group 3 appeared the cells in group 2 were ignored for the rest of the paper.
So the memory idea is not dead yet.